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Exact(6)
Depolarization due to loss of mitochondrial membrane potential causes the aggregates to dissolute into the monomeric forms.
Accordingly, the change of the electrical membrane potential causes the depolarization of the postsynaptic neuron that opens the voltage-gated ion channel of the NMDAR and consequently results in an increase of Ca2+ concentration that can be further enhanced through Ca2+ inward flux through L-type voltage-gated calcium channels (VGCCs) [53 57].
However, an intact mitochondrial membrane potential causes the positively charged dye to accumulate in the mitochondria where it aggregates to form a red fluorescent dimer.
The loss of mitochondrial membrane potential causes release of cytochrome-C and activation of caspase pathways that causes apoptotic detachment of renal cells.
The accumulation of solvents in the membrane destroys the membrane barrier, increases permeability, impairs energy transduction by dissipation of the membrane potential, causes dysfunctions of membrane proteins such as transport and signaling, and finally results in cell death (Ramos et al. 2002; Sikkema et al. 1995).
NO has been implicated as the major mediator of endothelium-dependent relaxation, but EDHF also plays an important role in regulating vascular tone and vasoreactivity, particularly in resistance blood vessels, where a small change in membrane potential causes a significant change in diameter [ 25].
Similar(54)
The transport of ions across the membrane can be related to the membrane potential caused by concentration gradient of an electrolyte impressed upon the membrane.
Ionophores that dissipate the mitochondrial membrane potential cause mitochondrial fragmentation, owing to an inhibition of mitochondrial fusion [49], [50].
Being shorter than the average inter-spike interval, the AHP has little effect on integration time and spike timing, which instead is entirely determined by fluctuations in membrane potential caused by the barrage of inhibitory and excitatory synaptic activity.
The occurrence of MPT induction in a particular mitochondrion is clearly identified by the instantaneous (<1 s) drop in its TMRM fluirescence to background level signifying the immediate and complete dissipation of mitochondrial membrane potential causing the loss of its sequestered dye.
Concentrations of inhibitor that caused no significant effect on pyramidal cell resting membrane potential, caused a marked and sustained membrane depolarization in fast-firing interneurons.
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